Left ventricular afterload and aortic input impedance: Implications of pulsatile blood flow☆

The structure and function of central arteries change throughout the lifetime of humans and animals. Since atherosclerosis and hypertension are prevalent in epidemic proportion among older persons, it is reasonable to hypothesize that specific mechanisms that underlie the arterial substrate that has been altered by an “aging process” are intimately linked to arterial diseases. Indeed, recent studies reveal a profile of arterial cell and matrix properties that emerges with advancing age within the grossly normal appearing aortic wall of both animals and humans. This profile is proinflammatory, and is manifested by intimal infiltration of fetal cells, increased production of angiotensin II (Ang II)-signaling pathway molecules, eg, matrix metalloproteases (MMPs), and monocyte chemoattractant protein (MCP-1), transforming growth factor B1 (TGF-β1), enhanced activation of MMPs, TGF-β, and NADPH oxidase, and reduced nitric oxide (NO) bioavailability. This profile is similar to that induced at younger ages in experimental animal models of hypertension or atherosclerosis. In humans, this proinflammatory state, which occurs in the absence of lipid deposition, appears to be attributable to aging, per se. Other well known human risk factors, eg, altered lipid metabolism, smoking, and lack of exercise, interact with this arterial substrate that is altered by aging and render the aging human artery fertile soil for facilitation of the initiation and progression of arterial diseases. Therapies to reduce or retard this age-associated proinflammatory state within the grossly appearing arterial wall central arteries, in addition to slowing arterial aging, per se, may have a substantial impact on the quintessential age-associated arterial diseases of our society.

Deux moniteurs permettant le monitorage du débit cardiaque (QC) ont été évalués : Vigilance™ (Lab. Baxter) associe mesures intermittente (QCTD Vig) et continue (QCc Vig) par thermodilution artérielle pulmonaire et requiert un cathéter artériel pulmonaire ; PICCO™ (Lab. Pulsion) permet le calcul du QC par l'analyse continue de la courbe de pression artérielle (QCc Pic) et la mesure intermittente du QC par thermodilution artérielle trans-thoracique (QCTD Pic), utilisé pour calculer un facteur de calibration nécessaire à l'estimation du QCc Pic. Les courbes sont recueillies par un cathéter artériel fémoral. Cette étude avait pour buts : 1) de comparer les deux méthodes, 2) de déterminer les situations pouvant compromettre la fiabilité de la technique du contour de pouls. Parmi les 301 mesures simultanées du QC réalisées chez 10 patients de réanimation, 44 paires réalisées au décours d'une calibration pendant une période d'extrasystoles ou après l'introduction de drogues vasoactives, sont très discordantes. La comparaison (régressions linéaires, agrément de Bland et Altmann) porte sur 257 couples de mesures. Les valeurs de QCc Pic et QCc Vig sont respectivement de 7,8±3,04 et 7,2±2,63 l/min⁻¹. La corrélation est excellente (r=0,94, p<10⁻⁴). Le biais est à0,5±1,06 l.min⁻¹ traduisant une surestimation du QC avec le moniteur PICCOTM (7 % du QC moyen) et l'intervalle de confiance est assez large. Dans 9 cas sur 10, il existe une corrélation individuelle entre les deux méthodes (corrélation des rangs de Spearman). Pour les QC inférieurs à 8 l.min⁻¹ (n=180), le biais est plus faible (0,22±0,66 l.min⁻¹). Par ailleurs, les 108 couples de mesures simultanées du QC obtenus par les techniques intermittentes de thermodilution sont bien corrélées, 8,1±3,2 l.min⁻¹ pour PICCO™ et 7,4±2,7 l.min⁻¹ pour Vigilance™ ; le biais représente 9,8 % du QC moyen (0,76±0,86 l.min⁻¹). Au total, l'agrément entre les deux méthodes de mesure du QC continu est correct, les valeurs fournies par le contour de pouls étant cependant plus élevées. La surestimation de QCTD Pic par rapport à QCTD Vig explique en partie les différences, le QCTD Pic étant intégré au facteur de calibration. La cause est une déperdition thermique liée aux sites de recueil différents. Elle est quantifiable et peut être intégrée au logiciel. Enfin, la survenue d'extrasystoles lors de la calibration invalide la mesure du QC par le moniteur PICCO™ et l'introduction de drogues vasoactives nécessite une nouvelle calibration.

Two devices for continuous cardiac output (CO) monitoring at patient bedside were evaluated. Vigilance™ monitor (Baxter Lab.) provides CO measurements by intermittent bolus (TDCO Vig) and continuous thermodilution (CCO Vig) methods, curves are both collected using a pulmonary artery catheter ; PICCO™ monitor (Pulsion Lab.) also provides continuous CO by pulse contour analysis (CCO Pic) and intermittent trans-thoracic thermodilution CO measurements (TDCO Pic), which is used to calculate a calibration factor for further beat-to-beat estimations of CCO Pic. Both systemic arterial pressure and thermodilution curves are collected using a femoral arterial catheter. The objectives of the study were : 1) to compare both methods, 2) to identify the situations possibly responsible for a poor reliability of the pulse contour method. CO measurements (n=301) were recorded simultaneously with both devices in 10 ICU patients : 44 conflicting data pairs, measured after vaso-active drugs initiation or following a calibration procedure performed during cardiac arythmia, were excluded. 257 data pairs for continuous CO measurements were compared using linear regressions and Bland-Altman plots method. Mean values for CCO Vig and CCO Pic were 7,3±2,63 and 7,8±3,04 l.min⁻¹ respectively, and the correlation was significant (r=0,94, p<10⁻⁴). The average difference (bias) was 0,5± 1,06 l.min⁻¹, i.e 7 % overestimation of CO by CCO Pic, and the 95 % confidence interval was large. For 9 among 10 patients the correlation between CCO Vig and CCO Pic was good (Spearman test). For CO values less than 8 l.min⁻¹, the bias and 95 % confidence interval were smaller (0,2±0,66 l.min⁻¹, n=180). Moreover, 108 data pairs for intermittent CO measurements were collected. The correlation between TDCO Vig (7,4±2,7 l.min⁻¹) and TDCO Pic (8,1±1,06 l.min⁻¹) was significant (r=0,97, p<10⁻⁴). The bias was 0,76±0,86 l.min⁻¹ and could be related to a thermal loss between pulmonary and femoral arterial collection. On the whole, the agrement between both continuous CO measurments is acceptable. Since TDCO Pic is used for CCO Pic calibration, the difference between the two CO continuous methods could be partly explained by an overestimation of TDCO Pic. Consequently, the software calibration process should be refined. Moreover, we identified two situations that are responsible for erroneous values of CCO Pic and require a new calibration : cardiac arythmia during PICCO™ calibration, vaso-active drugs initiation.